Fractional Excretion Of Magnesium Research Articles

Hypomagnesaemia is absent in children with autosomal dominant polycystic kidney disease

Hypomagnesaemia is present in 40-50% of children with autosomal dominant renal cysts and diabetes syndrome (RCAD). On the contrary, the prevalence of hypomagnesaemia in children with autosomal dominant polycystic kidney disease (ADPKD) has never been examined. We aimed to investigate whether hypomagnesaemia is present in children with polycystic kidney diseases. Children with cystic kidney diseases were investigated in a cross-sectional study. Serum concentrations of magnesium (S-Mg) and fractional excretion of magnesium (FE-Mg) were tested. Fifty-four children with ADPKD ( n = 26), autosomal recessive polycystic kidney disease (ARPKD) ( n = 16) and RCAD ( n = 12) with median age of 11.2 (0.6-18.6) years were investigated. Hypomagnesaemia (S-Mg < 0.7 mmol/L) was detected in none of the children with ADPKD/ARPKD and in eight children (67%) with RCAD. Median S-Mg in children with ADPKD/ARPKD was significantly higher than in children with RCAD (0.89 vs. 0.65 mmol/L, P < 0.01). The FE-Mg was increased in 23% of patients with ADPKD/ARPKD (all had chronic kidney disease stages 2-4) and in 63% of patients with RCAD, where it significantly correlated with estimated glomerular filtration rate (r = -0.87, P < 0.01). Hypomagnesaemia is absent in children with ADPKD or ARPKD and could serve as a marker for differential diagnostics between ADPKD, ARPKD and RCAD in children with cystic kidney diseases of unknown origin where molecular genetic testing is lacking. However, while hypomagnesaemia, in the absence of diuretics, appears to rule out ADPKD and ARPKD, normomagnesaemia does not rule out RCAD at least in those aged <3 years.

Longitudinal Study of the Role of Epidermal Growth Factor on the Fractional Excretion of Magnesium in Children: Effect of Calcineurin Inhibitors.

Background: It was shown in animal models and adults that the epidermal growth factor (EGF) is involved in the pathophysiology of calcineurin inhibitor (CNI) induced renal magnesium loss. In children, however, the exact mechanism remains unclear, which was set as the purpose of the present study. Methods: Children with nephrotic syndrome and renal transplant children treated with CNI (n = 50) and non-CNI treated children (n = 46) were included in this study. Urine and serum samples were collected at three time points to determine magnesium, creatinine, and EGF. The magnesium intake was calculated from a food frequency questionnaire. Results: Serum Mg2+ and urinary EGF/creatinine were significantly lower in the CNI treated children, with significantly more CNI-treated children developing hypomagnesaemia. In the latter patients, the fractional excretion of magnesium (FE Mg2+) was significantly higher. Urinary EGF, age, renal function, and serum magnesium were independent predictors of the FE Mg2+. Only 29% of the children reached the recommended daily intake of magnesium. The magnesium intake did not differ between hypomagnesemic and normomagnesemic patients and was not a predictor of the FE Mg2+. Conclusions: In CNI-treated children who developed hypomagnesemia, the FE Mg2+ was increased. The urinary EGF concentration, age, and renal function are independent predictors of the FE Mg2+.

Fractional excretion of magnesium and kidney function parameters in nondiabetic chronic kidney disease

Elevated fractional excretion of magnesium (FEMg) is a noninvasive biomarker of kidney damage, but its association with kidney functional parameters in nondiabetic chronic kidney disease (CKD) patients has not been sufficiently explored thus far. We enrolled 111 adult patients with nondiabetic CKD and 30 controls. To precisely investigate kidney function, the following parameters were assessed measured glomerular filtration rate (mGFR), effective renal plasma flow (ERPF), Cystatin C, albuminuria, and fractional excretion of magnesium (FEMg). All the CKD patients were divided into two groups according to the values of mGFR (mL/min/1.73m2): the first group consisted of those with GFR≥ 60mL/min/1.73m2, whereas the second group included those with GFR< 60mL/min/1.73m2. FEMg (%) was significantly higher in the group of nondiabetic patients with CKD compared to the healthy subjects [6.3 vs. 5.3 %, P=0.013]. There was also significant difference in the value of FEMg between the first and second groups of CKD patients. Increased FEMg was significantly correlated with all the investigated kidney function parameters, mGFR, ERPF, Cystatin C and albuminuria (r=-0.62; r=-0.60; r=0.77; r=0.39; p<0.01 for all). In multiple regression analyses based on observed parameters of kidney function, only cystatin C was independently and significantly associated with FEMg (multiple correlation coefficients: 0.738, p < 0.001)). Nondiabetic CKD patients with GFR< 60mL/min/1.73m2 have increased FEMg above 6.1% with 78.7 % specificity and 83.7% sensitivity. Highly significant association between kidney functional parameters and FEMg may indicate significance of this parameter in clinical practice.

A population-based approach to assess the heritability and distribution of renal handling of electrolytes

The handling of electrolytes by the kidney is essential for homeostasis. However, the heritability of these processes, the first step in gene discovery, is poorly known. To help clarify this, we estimated the heritability of serum concentration, urinary excretion, renal clearance, and fractional excretion of sodium, potassium, magnesium, calcium, phosphate, and chloride in a population-based study. Nuclear families were randomly selected from the general population in Lausanne, Geneva, and Bern, Switzerland, and urine collected over 24-hour periods. We used the ASSOC program (S.A.G.E.) to estimate narrow sense heritability, including sex, age, body mass index, and study center as covariates in the model. The 1128 participants, from 273 families, had a mean age of 47 years, body mass index of 25.0 kg/m2, and an estimated glomerular filtration rate (CKD-EPI) of 98 mL/min/1.73 m2. The heritability of serum concentration was highest for calcium, 37% and lowest for sodium, 13%. The heritability of 24-hour urine clearances, excretions, and fractional excretions ranged from 15%, 10%, and 16%, respectively, for potassium to 45%, 44%, and 51%, respectively, for calcium. All probability values were significant. The heritability for phosphate-related phenotypes was lower than that for calcium. Thus, the serum and urine concentrations as well as urinary excretion and renal handling of electrolytes are heritable in the general adult population. The phenotypic variance attributable to additive genetic factors was variable and was higher for calcium. These results pave the way for identifying genetic variants involved in electrolyte homeostasis in the general population.

Relationship between Fractional Excretion of Magnesium and Renal Histology in Glomerulonephritis

Progressive pediatric glomerularnephroses can lead to tubulointerstitial fibrosis (TIF) and chronic kidney disease (CKD). Fractional excretion of magnesium (FEMg) is a sensitive tubular function test (Ref). FEMg correlates positively with TIF (Ref). The purpose of the study was to correlate FEMg with renal histolopathology in pediatric glomerular nephrosis (GN). Sixty three cases, between 1-12 years, of biopsy diagnosed GN were included purposively in this cross sectional study from November 2008 to April 2010. Cases were taken from Department of Paediatric Nephrology, Dhaka Shishu (Children) Hospital and Department of Paediatric Nephrology, National Institute of Kidney Diseases & Urology, Sher-e-Bangla Nagar, Dhaka, Bangladesh. Minimal change disease (MCD) was most common at 27% and remaining 73% were other than MCD. The mean FEMg in MCD was normal (1.81 0.34%) but in other than MCD as a group it was significantly elevated (7.60 ± 19.23%; p<0.001). and significantly elevated separately in diffuse mesangial proliferative glomerulonephritis (3.96 ± 1.06%; p<0.001), focal segmental glomerulosclerosis (9.99± 4.45%; p<0.01), focal segmental proliferative glomerulonephritis (4.63 ± 2.29%; p<0.05) and crescentic glomerulonephritis (17.74 4.93%; p<0.01).

Genotype/Phenotype Analysis in 67 Chinese Patients with Gitelman's Syndrome

Background: Gitelman's syndrome (GS) is an autosomal recessive renal tubular disorder, which is caused by the mutations in SLC12A3. This study was designed to analyze the characteristics of the genotype and phenotype, and follow-up in the largest group of Chinese patients with GS. Methods: Sixty-seven patients with GS underwent SLCl2A3 analysis, and their clinical characteristics and biochemical findings as well as follow-up were reviewed, aiming to achieve a better description of GS. Additionally, the association of genotype and phenotype was explored. Results: Forty-one different mutations were identified within these 67 GS patients, including 11 novel mutations and 5 recurrent ones. Typical hypocalciuria and hypomagnesemia were not found in 6 (9%) and 8 (11.9%) patients, respectively. Male patients and those harboring severe mutations in both alleles had significant higher urinary fractional excretion (FE) of potassium, magnesium and chlorine. In addition, there were 2 patients who had chronic kidney disease (estimated glomerular filtration rate <60 ml/min/1.73 m²) and 32 patients with abnormal glucose metabolism. Conclusions: We identified 41 mutations related to GS, containing 11 novel variants and 5 high-frequency ones, which should facilitate earlier and more accurate diagnosis of GS. FE of electrolytes in urine may be more sensitive in the phenotype evaluation and differential diagnosis than corresponding serum electrolytes. Hypokalemia and hypomagnesemia in GS were difficult to correct; however, spironolactone might be helpful for hypokalemia to some degree. Compared with normal people, patients with GS were at higher risk of developing type 2 diabetes.

Hypomagnesemia in Pediatric Heart Transplant Patients Treated with Tacrolimus.

We aimed to investigate the frequency of hypomagnesemia and urinary magnesium excretion in pediatric heart transplant recipients. In this study, 22 pediatric patients who underwent heart transplanted at a single center between March 2014 and April 2015 and who were treated with oral tacrolimus were analyzed prospectively. Serum magnesium, creatinine, and tacrolimus levels and total amount of urinary magnesium excretion were measured. Serum tacrolimus levels were measured 12 hours after the last dose of tacrolimus. Our patient group included 11 boys (50%) and 11 girls (50%) with a mean age of 16.72 ± 4.78 years. Serum tacrolimus levels were in the therapeutic range, with a mean of 1.48 ± 0.13 ng/mL (range, 1.2-1.69 ng /mL), mean fractional magnesium excretion was 8.59 ± 5.9% (range, 3%-22%), and 24-hour urinary magnesium excretion was 90.2 ± 62.95 mg/d. Hypermagnesuria was assessed in 80% of patients. We found 24-hour urinary magnesium excretion to be higher than normal in 27% of patients. There was no association between serum tacrolimus levels and serum magnesium levels or urinary magnesium excretion. Serum magnesium levels should be periodically measured in pediatric heart transplant patients treated with tacrolimus.

Lipid-based nutrient supplements containing vitamins and minerals attenuate renal electrolyte loss in HIV/AIDS patients starting antiretroviral therapy: A randomized controlled trial in Zambia

Advanced HIV infection combined with undernutrition and antiretroviral therapy (ART) places HIV/AIDS patients at high risk of electrolyte abnormalities and increased morbidity and mortality. Here, in a sub-study of a large published randomized trial, we evaluated if nutritional supplements will help curtail renal electrolyte loss in HIV/AIDS patients starting ART. 130 malnourished HIV-positive patients referred for ART received lipid-based nutrient supplements alone (LNS, n=63) or together with vitamins and minerals (LNS-VM, n=67). Serum and spot urine samples were collected and assayed for creatinine, potassium, magnesium and phosphate concentrations at baseline and after 12 weeks of ART, and fractional excretion and reabsorption were calculated using standard equations. Eighteen (28.6%) patients from the LNS and 16 (23.9%) from LNS-VM groups died, most during the referral interval before starting ART. Phosphate excretion at baseline, was high in both LNS (mean±SD: 1.2±0.6mg/mg creatinine) and LNS-VM (1.1±0.8mg/mg creatinine) groups relative to normal physiological ranges. Phosphate excretion remained high in the LNS group (1.1±0.41mg/mg creatinine) but significantly decreased in the LNS-VM group (0.6±0.28mg/mg creatinine; p<0.001) after 12 weeks of ART. This difference is probably explained by increased renal tubular reabsorption of phosphate in the LNS-VM group (88.3±5.7%) compared to the LNS group (76.6±8.9%). The fractional excretion of potassium (FEK) was not significantly different at baseline between the two groups (p=0.69) but the values were above normal physiological ranges (i.e. >6.4%) reflecting renal potassium wasting. However, FEK was significantly lowered in the LNS-VM group (6.2±3.4%) but not in the LNS group (12.8±4.7%) after 12 weeks of ART (p<0.001). Finally, the fractional excretion of magnesium was not significantly different between the two groups at baseline (p=0.68) and remained unchanged within normal physiological ranges at 12 weeks of ART (p=0.82) in both groups. The LNS-VM regimen appeared to offer protection against phosphate and potassium loss during HIV/AIDS treatment. This offers potential opportunities to improve care and support of poorly nourished HIV-infected patients in resource-limited settings. www.pactr.org ID number: PACTR201106000300631.

Fractional excretion of magnesium, a marker of aminoglycoside induced nephrotoxicity in neonates.

Aminoglycoside is a widely used antibiotic in neonatal age group at hospital setting in Bangladesh. It has underlying side effect and toxicity which is mostly unseen and ignored. The aim of the study was to evaluate the nephrotoxic effect of aminoglycoside in neonates. This study was conducted in fifty hospital admitted neonates of Dhaka Shishu Hospital from January 2012 to December 2013. Serum creatinine, blood urea nitrogen, and fractional excretion of magnesium (FEMg) were measured before starting and after seven days of aminoglycoside treatment. Statistical analyses of the results were obtained by window-based computer software devised with Statistical Packages for Social Sciences (SPSS version 16). Statistical tests for significance of difference were done using Student's paired t-test. Serum creatinine and blood urea nitrogen were not significantly changed after drug administration (P = 0.092, P = 0.247, respectively). None of the neonates in our study group had abnormal serum creatinine and blood urea nitrogen after aminoglycoside therapy. FEMg was significantly increased (P <0.001) after aminoglycoside treatment. In this study, conventional renal function test such as blood urea and serum creatinine did not reflect the nephrotoxicity of aminoglycoside. However, a biomarker of tubular damage, FEMg detected nephrotoxicity of aminoglycoside therapy.

Water, electrolytes, and acid-base alterations in human immunodeficiency virus infected patients.

The clinical spectrum of human immunodeficiency virus (HIV) infection associated disease has changed significantly over the past decade, mainly due to the wide availability and improvement of combination antiretroviral therapy regiments. Serious complications associated with profound immunodeficiency are nowadays fortunately rare in patients with adequate access to care and treatment. However, HIV infected patients, and particularly those with acquired immune deficiency syndrome, are predisposed to a host of different water, electrolyte, and acid-base disorders (sometimes with opposite characteristics), since they have a modified renal physiology (reduced free water clearance, and relatively increased fractional excretion of calcium and magnesium) and they are also exposed to infectious, inflammatory, endocrinological, oncological variables which promote clinical conditions (such as fever, tachypnea, vomiting, diarrhea, polyuria, and delirium), and may require a variety of medical interventions (antiviral medication, antibiotics, antineoplastic agents), whose combination predispose them to undermine their homeostatic capability. As many of these disturbances may remain clinically silent until reaching an advanced condition, high awareness is advisable, particularly in patients with late diagnosis, concomitant inflammatory conditions and opportunistic diseases. These disorders contribute to both morbidity and mortality in HIV infected patients.

Prevention of amphotericin B nephrotoxicity through use of phytotherapeutic medication.

Objective To evaluate the effect of diosmin and hesperidin flavonoids in the prevention of amphotericin B nephrotoxicity, through an experimental model on rats. Method Adult, male Wistar rats were distributed into the following groups: saline; diosmin hesperidin (animals that received 50 mg/kg of diosmin hesperidin, drinking water, for ten days); amphotericin B (animals that received 15 mg/kg/day of amphotericin B through intraperitoneal treatment for five days); amphotericin B+diosmin hesperidin. Renal function, fractional excretion of sodium; potassium and magnesium and oxidative metabolites were evaluated. Results Treatment with amphotericin B reduced renal function, as shown by the clearance of creatinine, increased tubular function markers and fractional excretion of sodium, potassium, magnesium and oxidative metabolites. Pre-treatment with diosmin hesperidin ameliorated clearance of creatinine and reduced tubular and oxidative injury. Conclusion Administration of amphotericin B resulted in reduction of renal function with tubular injury, and diosmin hesperidin showing an antioxidant protective effect on the kidneys.

Pathophysiology of Calcium, Phosphorus, and Magnesium Dysregulation in Chronic Kidney Disease.

Calcium, phosphorus, and magnesium homeostasis is altered in chronic kidney disease (CKD). Hypocalcemia, hyperphosphatemia, and hypermagnesemia are not seen until advanced CKD because adaptations develop. Increased parathyroid hormone (PTH) secretion maintains serum calcium normal by increasing calcium efflux from bone, renal calcium reabsorption, and phosphate excretion. Similarly, renal phosphate excretion in CKD is maintained by increased secretion of fibroblast growth factor 23 (FGF23) and PTH. However, the phosphaturic effect of FGF23 is reduced by downregulation of its cofactor Klotho necessary for binding FGF23 to FGF receptors. Intestinal phosphate absorption is diminished in CKD due in part to reduced levels of 1,25 dihydroxyvitamin D. Unlike calcium and phosphorus, magnesium is not regulated by a hormone, but fractional excretion of magnesium increases as CKD progresses. As 60-70% of magnesium is reabsorbed in the thick ascending limb of Henle, activation of the calcium-sensing receptor by magnesium may facilitate magnesium excretion in CKD. Modification of the TRPM6 channel in the distal tubule may also have a role. Besides abnormal bone morphology and vascular calcification, abnormalities in mineral homeostasis are associated with increased cardiovascular risk, increased mortality and progression of CKD.

Clinical significance of fractional magnesium excretion (FEMg) as a predictor of interstitial nephropathy and its correlation with conventional parameters.

Elevated urine Mg excretion and its correlation with histological damage in tubulo-interstitial nephropathy (TIN) were reported. Here we investigated the clinical significance of the fractional excretion of Mg (FEMg) for the prediction of TIN. We enrolled and assessed 94 adult patients with various renal diseases diagnosed principally by renal biopsy. Our stratified analysis based on the value of the conventional TIN parameter N-acetylglucosaminidase (NAG) excretion showed that the high-NAG index group (more than median value of NAG-to-Cr ratio, n=47) demonstrated significantly high FEMg values (p=0.017). A univariate analysis revealed a significant correlation between the FEMg and the NAG index (R=0.60) but not for other parameters. A multivariate regression analysis confirmed the significance of the FEMg as an effective predictor of the NAG index. The FEMg showed a significant correlation with the estimated glomerular filtration rate (eGFR) in the patients with eGFR≤30mL/min. The correlation of FEMg with the NAG index was not observed in the primary glomerulonephritis patients but was apparent in the patients with hypertensive nephrosclerosis or interstitial nephritis. Our findings may indicate that the combination of the FEMg and the NAG index can provide a specific, sensitive assessment for TIN in patients without renal insufficiency.

Retrospective cohort study of familial hypomagnesaemia with hypercalciuria and nephrocalcinosis due to CLDN16 mutations.

Familial hypomagnesaemia with hypercalciuria and nephrocalcinosis (FHHNC) is a rare autosomal recessive tubular disorder exhibiting a high risk for progressive chronic kidney disease (CKD). This is a retrospective multicentre study of 25 paediatric cases with FHHNC in Poland. Median age at diagnosis was 4 years and median follow-up time was 4.8 years. All cases of FHHNC carried recessive mutations in CLDN16. The founder mutation in CLDN16, Leu151Phe, was the most frequent cause of FHHNC in Polish patients, with 13 (52%) cases being homozygous and 5 (20%) carrying Leu151Phe allele in compound heterozygosity. All cases showed nephrocalcinosis, increased urinary fractional excretion of magnesium and hypercalciuria. Other disease features included hypomagnesaemia (76%), hyperparathyroidism (76%), hyperuricaemia (56%) and hypocitraturia (60%). Treatment with thiazides effectively reduced hypercalciuria in most cases. During follow-up, renal function declined in 60% of patients; 12% of patients reached CKD stage 3 or 4 and one patient developed end-stage renal failure. We report one of the largest cohorts of FHHNC cases caused by CLDN16 mutations. A missense variant of CLDN16, Leu151Phe, is the most common mutation responsible for FHHNC in Poland. Additionally, we found that normomagnesaemia does not exclude FHHNC and the calculation of fractional excretion of Mg can be diagnostic in the setting of normomagnesaemia. We also demonstrate the efficacy of a treatment with thiazides in terms of hypercalciuria in the majority of patients.

Valor diagnóstico de la excreción fraccional de minerales para evaluar el metabolismo del calcio, magnesio y fósforo en el perro

The aim of this work was to establish reference values of the fractional excretion (FE) of calcium (Ca), phosphorus (P) and magnesium (Mg) in dogs, proposing a methodology for their obtention. The dogs were divided into groups SS: standard diet and CS: standard diet plus calcium supplement for 10 days. We observed increased plasma concentration of P, both fasting and postprandial, in CS respect to SS. More FECa in CS respect to SS in fasting and postprandial. SS showed a lower FEP and FEMg in fasting than postprandial, parameters that were stabilized in CS. (p<0.01). Thanks to the proposed methodology and the associated analysis of minerals we can see the lack of calcium in SS group despite having EFCa values that are at the bibliography.

Magnesium excretion and hypomagnesemia in pediatric renal transplant recipients

Background: We investigated magnesium excretion and rate of hypomagnesemia in pediatric renal transplant recipients. Method: The medical records of 114 pediatric renal transplant recipients were retrospectively evaluated. After exclusion of 23 patients, 91 patients were included in the study. We recorded serum magnesium levels at the time of measurement of urine magnesium wasting. Results: Mean serum magnesium levels were 1.73 ± 0.22 mg/dL and 38 of the patients (41%) had hypomagnesemia. There was a negative correlation between serum magnesium levels and estimated glomerular filtration rate and serum tacrolimus trough level (r = −0.215, p = 0.040 and r = −0.409, p = 0.000, respectively). Also, there was a statistically significant positive correlation between serum magnesium levels and transplantation duration (r = 0.249, p = 0.017). Mean fractional magnesium excretion was 5.9 ± 3.7% and 59 patients (65%) had high magnesium excretion. There was a significant negative correlation between fractional magnesium excretion and estimated glomerular filtration rate (r = −0.432, p = 0.001). There was a significant positive correlation between fractional magnesium excretion and serum creatinine (r = 0.379 p = 0.003). Conclusion: Patients with higher tacrolimus trough blood levels, lower glomerular filtration rate and at early posttransplant period had risk of hypomagnesemia.

Effect of dietary potassium supplementation on the calcium absorption capacity in the rumen and abomasum and fractional excretion of urinary minerals in sheep

The aim of this study was to determine the effect of potassium (K) supplementation on the calcium (Ca) absorption capacity from the rumen and abomasum of sheep. The Ca absorption capacity from the rumen and abomasum of sheep was measured using stable strontium (Sr) as a Ca-analogue tracer method. The sheep, cannulated at either the rumen or abomasum, were randomly allocated to one of two groups (control or K-supplemented) and fed in individual metabolism pens twice daily with a diet comprising oaten hay, lucerne chaff and barley fortified with or without potassium carbonate (K2CO3). The K content of the diet of the K-supplemented animals was 3.1% of dry matter compared with 1.4% for the control animals. The animals were fed their respective diets for a period of 2 weeks. The fractional absorption capacity (FC) of Ca was estimated before, during and after the treatment period. Supplementation with K decreased the FC of Ca in both the rumen and abomasum during treatment and increased the FC of Ca in the abomasum post-treatment. Supplementation with K also increased the fractional excretion of K in the urine, but decreased the fractional excretion of Ca and magnesium (Mg) (P &lt; 0.05), showing that K supplementation significantly affected Ca and Mg metabolism. Results suggest that renal conservation of Ca and Mg is an important mechanism controlling the Ca and Mg pool for vital functions of the body. In times of high demand for these minerals during lactation and pregnancy, high K in the diets may predispose sheep to hypomagnesaemia and hypocalcaemia, which in turn will have a negative impact on productivity and economic returns.

Correlation of fractional excretion of magnesium with steroid responsiveness in children with nephrotic syndrome.

Steroid-resistant nephrotic syndrome (SRNS) patients are candidates for other alter-native drug regimes, and the non-responsiveness to steroid is more common among glomerulo-nephritides other than minimal change disease. Without performing biopsy and proper renal histology, progression of the disease cannot be assessed. Fractional excretion of magnesium (FE Mg) has been found to correlate directly with various renal histologies. The aim of this study is to evaluate the relationship of FE Mg in children with the histological pattern in SRNS. In this prospective observational study, 40 children of nephrotic syndrome, both with the first episode as well as relapse, aged 1-12 years were included in the study. Of them, 20 were steroid-responsive cases and 20 were steroid-resistant cases. FE Mg was determined in all the patients and renal histology was performed in the steroid-resistant cases. A correlation was found between FE Mg and renal histology. Data were analyzed in SPSS program version-16. Comparison of two groups was performed by the Fisher exact test and unpaired t test. P-value less than 0.05 were considered to be significant. The results of histo-pathology showed that the mean difference in FE Mg was significant (P <0.001), as FE Mg was 7.0 ± 2.3% in mesangiocapillary glomerulonephritis, 6.9 ± 1.3% in focal segmental glomerulosclerosis, 4.7 ± 0.6% in immunoglobulin M nephropathy, 4.5 ± 1.2% in focal segmental proliferative glomerulo-nephritis, 4.4 ± 1.6% in minimal change disease, 4.2 ± 0.4% in diffuse mesangial proliferative glome-rulonephritis and 3.8 ± 1.3% in mesangial proliferative glomerulonephritis. There was a statistically significant difference between FE Mg in steroid-resistant nephrotic syndrome (4.9 ± 1.9) and steroid-responsive syndrome (1.2 ± 0.3). FE Mg is a simple, minimally invasive screening marker for SRNS, and is an early predictor of clinical outcome. It can be considered as an initial investigation where biopsy cannot be performed or indications are not clear.

Ankyrin-3 is a novel binding partner of the voltage-gated potassium channel Kv1.1 implicated in renal magnesium handling

The voltage-gated potassium channel, Kv1.1, was recently identified as a causative gene in isolated dominant hypomagnesemia. The channel is situated in the distal convoluted tubule, where it participates in maintaining a favorable electrical gradient for driving magnesium ion into the cell through the transient receptor potential melastatin 6 channel. Pull-down experiments coupled to mass spectrometry using the carboxy-terminal domain of Kv1.1 as bait were used in mouse kidney lysates. Ankyrin-3 (ANK3) was identified as a binding partner of Kv1.1 and was enriched in isolated distal convoluted tubules as compared to whole kidney. Electrophysiology studies performed in HEK293 cells expressing Kv1.1 showed that ANK3 significantly inhibited Kv1.1-mediated currents (267 compared to 125 pA/pF) for control and ANK3, respectively. Finally, to evaluate a potential role of ANK3 in magnesium handling, the intrarenal abundance of ANK3 was measured in mice fed a low-, normal-, or high-magnesium diet for 10 days. Mice maintained on high dietary magnesium significantly doubled their fractional urinary excretion of magnesium, which coincided with a 1.8-fold increase in the renal expression of ANK3 compared to mice on a normal- or low-magnesium diet. Thus, our observations demonstrate a novel role for ANK3 in modulating the biophysical properties of Kv1.1. Such regulation appears to be particularly important in conditions of high dietary magnesium.

The Role of Distubances of Phosphate Metabolism in Metabolic Syndrome

Abstract Background and Aims: Metabolic syndrome represents a cluster of cardiovascular risk factors and reached epidemic proportions. It was hypothesized that disturbances in phosphate metabolism may represent a feature of the metabolic syndrome. The aim of the study was to investigate the relationship between phosphate levels and the presence of metabolic syndrome components, as well as the putative mechanism for reduced phosphate level in metabolic syndrome. Materials and Methods: We enrolled 155 subjects: 64 with metabolic syndrome and 91 controls. Biochemical parameters of the metabolic syndrome study population were compared with the healthy population. Results: Patients with metabolic syndrome showed significantly lower phosphate (46%) and magnesium levels compared with controls (22.7%) (p&lt;0.001). Women showed significantly greater serum phosphate levels than men (3.32 mg/dl versus 3.18 mg/dl) (p&lt;0.03). Serum magnesium levels did no differ significantly between men and women. Fractional phosphate excretion rates in patients with metabolic syndrome were similar with controls (10.1±10.2% vs 13.1±9.9%), as well as fractional magnesium excretion (3.1±1.6% vs 2.8±1.3%). Conclusions: Patients with metabolic syndrome show significantly lower phosphate and magnesium concentrations compared to controls. This reduction is likely to be attributed to internal redistribution of phosphate and is more pronounced as the number of components of metabolic syndrome increases